Subjects with a total isolated deficiency of growth hormone exhibit hypercholesterolemia and hypertriglyceridemia which is baffling and unexplained. The majority of these patients have abnormal glucose tolerance which does not correlate with the presence or absence of abnormal serum lipids. Despite the metabolic resemblance of the growth hormone deficient state to both diabetes mellitus and hyperlipemic states, (1) microangiopathic lesions do not appear in HGH deficient subjects, and (2) pathological involvement of larger arteries appears to be uncommon. We wish to document this latter observation more thoroughly and to determine if this knowledge can be used for controlling atherosclerosis and arteriolersclerosis in man. We will (1) verify that a chronic deficiency of HGH prevents the evolution of clinically evident arterial disease, and (2) determine the manner in which HGH affects lipid and lipoprotein metabolism in man. For the latter studies, we will examine specifically the kinetics of cholesterol turn-over in the absence or presence of growth hormone and the molecular status of LDL in the growth hormone deficient state. We will likewise evaluate more thoroughly growth hormone secretion in hyperlipidemic patients (Types II and IV) as our preliminary data indicates a relative deficiency of growth hormone in these states.